Transcranial direct current stimulation - tDCS

Transcranial direct current stimulation is a type of nonivasive cortical modulations technique witch use low DC current in order 25-80uA/cm2(more in HD-tdcs) via skalp electrodes to change resitng potentials of neurones.This chanages depend of polarity of stimulation = orintation od el. field to the neurones,the anodal (+) stimulation increases the neuronal excitability and Cathodal (-) neuronal excitability.When positive stimulation causes a depolarization of the resting membrane potential, which increases neuronal excitability and allows for more spontaneous cell firing. When negative stimulation is delivered, the current causes a hyperpolarization of the resting membrane potential. This decreases neuron excitability due to the decreased spontaneous cell firing.TDCS also have neuroplastic effect Anodal tDCS could induce long-term potentiation (LTP) through increased pre-synaptic activity coupled with postsynaptic depolarisation; conversely, cathodal tDCS could induce long-term depression (LTD) through reduced presynaptic discharge and postsynaptic hyperpolarisation.

Safety considerations for tDCS

Numerous studies verify that low-intensity transcranial stimulation is safe
for use in humans and that it is linked with only rare and relatively minor
adverse effects (Poreisz, Boros, Antal, & Paulus, 2007). tDCS does not
elevate the serum levels of molecular markers of neuronal injury such as
neuron-specific enolase (Nitsche & Paulus, 2001) or N-acetyl-aspartate
(Rango et al., 2008). Furthermore, both contrast-enhanced MRI and
EEG studies have found no pathological changes associated with application
of tDCS (Iyezr et al., 2005; Nitsche, Niehaus et al., 2004).
Additionally, no instances of epileptic seizures caused by tDCS have been
observed in humans (Poreisz et al., 2007). In fact, pulsed transcranial stimulation
has been correlated with an antiepileptic effect in rats (Liebetanz
et al., 2006) and a previous tDCS study in patients with refractory
epilepsy did not show an increase in seizures or EEG-epileptiform discharges
(Fregni, Thome-Souza et al., 2006). The most common side
effects observed with tDCS are mild tingling (70.6%), moderate fatigue
(35.3%), sensations of light itching (30.4%), slight burning (21.6%), and
mild pain (15.7%) under the electrodes (Poreisz et al., 2007).
Less commonly, some subjects report headache (11.8%), trouble concentrating
(10.8%), nausea (2.9%), and sleep disturbances (1.0%) (Poreisz
et al., 2007). Skin lesions in the form of burns following administration of
tDCS have been reported (Palm, 2008). Visual sensations associated with
turning the stimulation on or off have occurred in a small number of
cases, but this can be avoided by slowly changing the current level at the
start and end of stimulation. tDCS delivered at a level of 2 mA and
administered according to current stimulation guidelines (Nitsche, 2008)
has been shown to be safe for use in both healthy volunteers (Iyer et al.,
2005) and patients with neurological injury (Boggio, Nunes et al., 2007).
Using a rat model, researchers investigated the safety limits of extended
cathodal tDCS and found the charge density threshold to be two orders
of magnitude greater than the charge currently administered in humans
(Liebetanz et al., 2009). The safety of tDCS use in pregnant women and
children, however, has not yet been investigated.

Step bay step way to understaning a tDCS

this part only shows various factors influencing the effect in end you must consider all this factors at once with all its concetivity and dependences

Stimulation current

In studes you find value 1 or 2 mA but what this tell you about effect of stimulation? Hard trouth is : almoust nothing ,without furteher information is this value useles.You need this value to count other more precize data.

Current density on electrodes

What this means, how to count it

This means current from the device devided by surface volume of electrodes.Moustly write in this manner uA/cm2 or mA/cm2 in some sudy you may find A/m2.

uA means 0,001 mA

to count current desity you need surface area and current

for istance electrode 6x6cm have 36cm2 surface and with 1mA current source will have a current density 1/36= 0,027mA/cm2 =27uA/cm2

electrode size in studies is about 15-100cm2 (for standard tdcs) in most of them 25-35cm2

Current density in electrode and safety

Studies have been completed to determine the current density at which overt brain damage occurs in rats. It was found that in cathodal stimulation, a current density of 142.9 A/m2 delivering a charge density of 52400 C/m2 or higher caused a brain lesion in the rat. This is over two orders of magnitude from what is currently being used. (14,2mA/cm2 )
The current density produced by present tDCS protocols ranges between 0.029 and 0.08 mA/cm2.It seem like safety measure not strict limit.Some experimental HD-TDCS to use 500uA/cm2 and test even 2000uA/cm2 withot harm ( but there is necessary to use special electrodes, gels and skin preparation).For normal tDCS is be good not to exceed 80uA/cm2 until be aviable more info about safety.
We must also distinguish dangerous current density for the brain and the skin.
Higher current density does not necessarily mean that the effect will be stronger.
*needed more info about this 14,2mA/cm2 the validity of this information is very limited if we not know precize methdology of measurmnet the change in value can be few orders!!

Current density in electrode and effect

Brain function under the electrode site is enhanced by roughly 20 to 40% when the electrode current density exceeds 40 µa/cm2 (260 µa/inch2).

Cathode -

reduces brain function under the electrode site by 10 to 30% at the fore-mentioned current density.

this is very oversimplified !!! read further section for more info

without information about placemet and size of electrode is this value almosut useless

The brain-stimulating electrode is called the active electrode, whereas the circuit-completing inactive electrode is called the reference electrode. In most of the studies, the reference has been placed over the contralateral orbit (above the left or right eye) to avoid negative effects from it. However, the studies never looked at the inhibiting effects that the reference electrode might have had on the prefrontal lobe. Some recent studies and in particular a study by Nitsche, et al., (2007) show that it is better to have a small stimulating electrode and large reference electrode.
electrodes effect must be considered as a whole, the reference electrode always affect the active one
larger reference electrode minimalize the unwanted effect,current density below 27uA/cm2 is in some studies considered functional unefective.

this also not entirely true, it is oversimplified read further section for more info

my recomandation is use for the return electrode current below 20uA if it possible

Nitsche and Paulus found that a minimum current density of 17 µa/cm2 was needed to excite motor neurons. Studies involving other regions of the brain have suggested that 20 to 25 µa/cm2 are needed to excite neurons under the electrode. One depression study using anodal stimulation at F3 noted alleviated depression using 1 mA into a 35 cm2 electrode (28 µa/cm2). Iyer, et al., observed that when stimulating the left prefrontal cortex there was no effect on verbal fluency with a 1 mA current, but significant improvements at 2 mA (current density of 20 µa/cm2 vs 41 µa/cm2). Two depression studies by Boggio, et al., 2007; Boggio, et al., 2007) also used 2 ma.

the excite is very vague name i not shure what this means

is only for electrodes not cortex so the info means only if you use they electrode configuration you see this effects , for other areas and configuration the values may be very different

Edge effects

The high current density at an electrode edge is generally undesirable for safety reasons and may increase sensation during
transcutaneous stimulation.

Theory

study:Cutaneous perception during tDCS: Role of electrode shape and sponge salinity

WARNING in many studies scientist count wrong so read it carefully

if they want it in A/m2 that value is be 0,57 not 0,0057 its be better use 57uA/cm2

this 0,041A/m2 is in real 4,1A/m2 this means the max in graph is 410uA/cm2 (290uA/cm2,120uA/cm2)

Shunting

Large part of current is shunted by skin and also by lower level by skull and CSF.
The ammount of current reaching cortex is depend of current density on electrodes its sizes and placements nad also of skin a skull thickenes.
Current models dount count with skull anisotropy of conductivnes becouse is very hard get data for this model by MRI (it posible use CT).
* individual male scalp and skull thickness variation, which can be as high as 58% and
34% of the average, resulted in up to 76% and 20% changes of the
peak brain E-field, respectively

shunting value means how many times is current in the cortex lower than in skin

To quantify the shunting effect, we divided

the average maximum skin current density by the maximum
cortical current density, where the average maximum skin current
density was defined as the current density magnitude on the skin
for which at least 0.5 cm2 in area was covered and which was
not confined to the electrode boundary edge effects

Basic rules (for orintational values look to studies)

smaller electrode have = more shunting

electrode close together = more shunting

From one test:
Electrode density in the cortex, i try to count difference of current density with this configuration nad standart 35cm2 pads (its only orientational)
EKG electrode 3,14cm2 ,1mA , 318uA/cm2 ,+ on L-DLPFC and - on FT10 (left temporal below the hairline)

Role of size

normal 8,7uA/cm2

HD 21,5uA/cm2

Inresiting is current desity on electrode is be 11,21x higher but current density on top of the cortex only 2,47x
This also means the current density is be the same like in 2,5mA with standart 35cm2 pads.

The accuracy of these data is limited by several assumptions that were built into the model, such as the layered spherical geometry and the conductivity values used. However, since we are only calculating ratios (e.g., by what factor should the current be reduced when the electrode area is halved) as opposed to absolute values (e.g., what is the current density value at the target point), the results should not depend too strongly on those assumptions

Shunting

only a very rude aproximation

normal 8-9 uA/cm2 max

HD 12-13uA/cm2 max

If we consider size and shunting effect the current density will be only 1,5 higher than in standart 1mA/35cm2

Implants

In discusions on the net is apper idea use some implants to tDCS.There is many options easiest is usage of microdermal implant materil is may be problem ,titan is seem posile but need testing.From my point of view is adventages not overcome the risks in sub dermal implant is be focality the same.Another options (my idea) is drill hole to the skull but not whole way trught pus some lectrode in nad isolator of top of it this is may increase focality and lowering needed current.Last option requied electron direcly in brain or in top of it hereis risk much grater.Probably best in this case is be used some electrode array.Device can have inductive recharge or contact on the skin.Main problem is infamatory response from body cause bad healing and need to remove implant and many others.So in short is posible but current state is not worth a risk becouse wee not know much about effect of stimulation yet.

Hi-frequenci currents ,inereference currents

need more close look to it , if it work may provide better targeting, deeper stimulatin and large reduce in skin iritation.

betrer for CES than for tDCS

Current distribution in the brain

In previous part we considered cortex mainly like a plane and white matter like have same conductivyty on all places for uderstanding next parts we needed more precize models,i start with easiest less complex/acurate ones.

Cortex folding

Know folding is very important becouse change the current distirbution and effect of tDCS mainly depends on orientation of neuronal structures to the DC vector .
For now is not looking good for DIY tDCS projects this sentence desciping problem prety well:
Individual variability of the human cerebral cortex is a source of both fascination and frustration.

Folding patterns are relatively consistent in some regions (e.g.,the central sulcus) and much more variable in other, regions, including much of prefrontal and parieto-temporal cortex.

main sulci map

central sulcus , motor cortex

M1 area 4 position in the sulcus (usefull for radial/tangental field optimalization)

Interidividual variabality

50 brains of the ICBM database processed by BrainVISA after alignement in Talairach space

some part is more variable than other this info cam be used to aproximate the field orintation to neurones on this areas

I searching for more maps of folding variabylity

Averaged MRI models

Give only very limited info , if be better to compare many subject MRI and look for similarity nad variablity (idelay find models of this variabylity).

White matter conductivity anisotrophy

New models must count with anisotrophy of conductivyty of white matter caused by neuronal fibers
to measure this is used technique called Diffusion tensor imaging (DTI) its a kind of MRI in some papeer
named also DT-MRI.

The current flow
generally follows the path of least electrical impedance. Consequently,
compared to the isotropic model, current flow along theWMfibers
in the anisotropic model is denser and follows the fiber orientation. In
some cases the channeling of current along WM fiber tracts increases
the local E-field strength, but in other cases this effect is offset by the
lower impedance along the fibers, leading to reduced E-field strength.
The current may steer away from segments of increased impedance
resulting from the passage of WM fibers perpendicular to the current
flow. However, when current comes across wide stretches of fibers
perpendicular to its flow, the current cannot steer away and is forced
to cross this high impedance barrier, resulting in high E-field magnitude.
Thus, increased E-field strength in the anisotropic model compared
to the isotropic model can result from either concentration of
current flow along WM fibers that is not offset by the low impedance
along the fibers, or from increased impedance for current flow perpendicular
to WM fiber.

the same is be for cortex neurones orintation (fibers is smaller but current higher)

Computational models

more info about variables in and of this study:
Regional electric field induced by electroconvulsive therapy in a realistic finite
element head model: Influence of white matter anisotropic conductivity

Metods

The spherical and simplified geometry models do not fully account for tissue inhomogeneity and
anisotropy, and the complex geometries of head tissues, including orifices in the skull such as the auditory canals and the orbits.

Concentric sheres models

low-resolution realistically-shaped representations

MRI based models

MRI and DTI based models

its ECT not tDCS but current ditribution may be the same only field density is be much lower

they used MRI+DTI :) but here is big limitations of this study :( electrodes as point sources ,MRI was only acquired for the portion of the head

can good model but this is very limited they dount read how large effect is have size and palace elctrode to shunting and current to the cortex,also lower shunting by partial head model not add much to acuracy

Rescaling the current from Sadleir et al.'s (2010) and Parazzini et al.'s
(2011) anatomically-realistic tDCSmodels and converting current density
to E-field strength, the average of their reported median values is
2.5 V/cmand 2.7 V/cm, respectively.

Information

Current

A/m2 ,mA/cm2 ,uA/cm2

Field

V/m ,V/cm
study comparing head models for TMS found a ~51% increase of the maximum
E-field strength in the anatomically-realistic model compared
to simplified spherical models (

Orientation

Focality of stimulation

Stimulation Site

p0225 The location of the electrode placement in tDCS is critically important
because placement of the electrodes in different areas will result in distribution
of current density to those respective areas of the brain. Indeed,
imaging studies confirm that the polarizing effects of tDCS are generally
restricted to the area under the electrodes (Nitsche, Liebetanz et al., 2003;
Nitsche, Niehaus et al., 2004). Stimulation of motor cortex (M1), occipital
cortex (V1), somatosensory cortices, and dorsolateral prefrontal cortex
all have been shown to deliver site-specific and differential effects on a
gamut of cognitive, behavioral, psychosomatic, and electrophysiological
tests (Zaghi et al., 2010).Additionally, some evidence suggests that tDCS can have highly focal
effects. In a study examining the combined effects of tDCS and peripheral
nerve stimulation, Uy and Ridding (2003) optimized (using TMS) the
site of tDCS for the first dorsal interosseous muscle and observed significant
excitability changes for this muscle, but not the nearby abductor digiti
minimi and flexor carpi ulnaris muscles (Uy & Ridding, 2003). A
recent modeling study, however, has suggested that electric current might
actually have its peak between the two electrodes (Datta et al., 2009).

For example,
anodal tDCS of premotor cortex increases the excitability of the ipsilateral

*find studies and look at focality motor cortex (Boros, Poreisz, Munchau, Paulus, & Nitsche, 2008), and
stimulation of the primary motor cortex has inhibitory effects on contralateral
motor areas (Vines, Cerruti, & Schlaug, 2008). This supports the notion
that tDCS has a functional effect not only on the underlying corticospinal
excitability but also on distant neural networks (Nitsche et al., 2005).

Indeed, fMRI studies reveal that although tDCS has the most activating
effect on the underlying cortex (Kwon et al., 2008), the stimulation provokes
sustained and widespread changes in other regions of the brain as well
(Lang et al., 2005). EEG studies support these findings, showing that stimulation
of a particular area (e.g., frontal cortex) induces changes to oscillatory
activity that are synchronous throughout the brain (Ardolino, Bossi,
Barbieri, & Priori, 2005; Marshall, Molle, Hallschmid, & Born, 2004).
p0235 Hence, this evidence suggests that the effects of DC stimulation are
site-specific but not site-limited. That is, stimulation of one area will
likely have effects on other areas, most probably via networks of interneuronal
circuits (Lefaucheur, 2008). This phenomenon is not surprising
given the neuroanatomic complexity of the brain, but it raises interesting
questions as to: (1) how the effects are transmitted; and (2) whether the
observed clinical effects (e.g., pain alleviation) are mediated primarily
through the area of the cortex being stimulated or secondarily via activation
or inhibition of other cortical or sub-cortical structures (Boggio,
Zaghi, & Fregni, 2009; Boggio, Zaghi, Lopes et al., 2008). For instance
Roche et al. (2009) demonstrated that anodal tDCS of the motor cortex
modifies excitability at the level of the spinal cord by showing that tDCS
increases reflexive inhibition directed from the extensor carpi radialis to
flexor carpi radialis, which is mediated by inhibitory interneurons located
in the spinal cord (Roche, Lackmy, Achache, Bussel, & Katz, 2009).
Therefore, observed clinical effects from tDCS might be explained by
changes to several possible regions in the central nervous system (see
Table 12.1 for a summary of the effects of varying parameters of tDCS).

standart vs HD-tDCS focality

Neurones

Radman et al. (2009) in rat cortical neurons suggests that the soma of layer
V pyramidal cells are individually most sensitive to polarization by optimally
oriented subthreshold fields. Moreover, Radman et al. (2009) also
reveal that cortical layer V/VI neurons had the lowest absolute action
potential thresholds. This suggests that while the electric field induced by
tDCS likely has sensitizing effects at the dendrites of neurons in all six cortical
layers (Radman, Datta, Ramos, Brumberg, & Bikson, 2009), it is
the soma of the neurons in layers Vand VI that are most susceptible to the
polarizing and excitability modulating effects of tDCS (Radman, Ramos,
Brumberg, & Bikson, 2009).

TESHOLD

As a reference point, cortical current density
magnitudes are far lower than action potential thresholds: 0.079 to
0.20 A/m2 induced by tDCS as compared to 22 to 275 A/m2 required to
trigger an action potential (Tehovnik, 1996).

7,9-20uA/cm2 vs 220-2750uA/cm2

Orientation

Orientation of neuronal structures relative to the DC vector that determines the effect of tDCS.
spike depend on axonal orientation relative to the electric field vector. Axonal orientation determines whether the DC field is excitatory or inhibitory and dendritic orientation affects the magnitude, but not the overall direction, of the DC effect. These data suggest that tDCS may oppositely affect neurons in a stimulated cortical volume if these neurons are excited by oppositely orientated axons in a constant electrical field.

TODO: find whole study:

Contribution of axonal orientation to pathway-dependent modulation of excitatory transmission by direct current stimulation in isolated rat hippocampu

Non-neuronal

Astrocyte theory:

As a second – not contradictory – hypothesis, we would like to
propose the following speculation. While it is true that tDCS affects
the electrical properties of neurons, it could also affect the electrical
properties of astrocytes. Astrocytes greatly outnumber neurons and
occupy 25–50% of brain volume, so it is conceivable that they can be
polarized by tDCS. Astrocytes play a pivotal role in the regulation of
rCBF and its coupling with neuronal activity (Gordon et al., 2008;
Koehler et al., 2009). Recently, astrocytes have been proposed to also
play a role in long-term changes in synaptic efficacy and neurotransmitter
(glutamate) release (Perea and Araque, 2007). Astrocytes are
strongly coupled to one another by gap junctions. Such communication
is believed to mediate the coordinated action of adjacent
individual cells and equalizes their intracellular ion concentrations.
Application of direct current over distant parts of the brain can
polarize the strongly interconnected astrocyte network. Therefore,
astrocytes could play an important role in the mechanisms of the tDCS
after-effects in the human brain

Connections

For determinatin effect of tDCS we must consider not only areas where electric field affect neurones but also connections from this areas to other part of brain.
Large neuronal bundles its posible find by DT-MRI but this not enought we also need to know how affect each other its is concetion inbitory ,excitaory or bouth nad other more complex dependeces.

Intracortical Inhibition and Facilitation

With regard to intra-tDCS excitability changes, they found that anodal
tDCS did not induce cortical inhibition or facilitation, while cathodal
tDCS reduced facilitation. For the short-lasting after-effects, they found
that anodal tDCS reduced inhibition and enhanced facilitation, while
cathodal tDCS enhanced inhibition and reduced facilitation. Finally, for
the long-lasting after-effects anodal tDCS decreased inhibition for ISIs of
3 ms, while cathodal tDCS increased inhibition at ISIs of 2 ms and 5 ms.
Though for long-lasting effects the ISI of 15 ms condition did not show
modified facilitation, anodal tDCS increased facilitation at ISI of 10 ms,
while cathodal tDCS reduced facilitation.
p0260 These results suggest that intracortical inhibition and facilitation can
be modified by tDCS. For the short-lasting and long-lasting effects,
anodal tDCS can increase facilitation and decrease inhibition, while cathodal
tDCS can produce the opposite effect. While intra-tDCS facilitatory
effects are not observed for anodal stimulation, they are decreased for
cathodal stimulation.
*more in article

Transcallosal Inhibition

Fregni et al. (2005) investigated whether reduction of activity in the unaffected
hemisphere by cathodal tDCS would result in improved motor performance
due to decreased transcallosal inhibition. Indeed, they found that
cathodal stimulation of the unaffected hemisphere, as well as anodal
stimulation of the affected hemisphere, significantly improved motor
performance compared to sham tDCS (Fregni, Boggio, Mansur et al.,
2005). In a recent study of healthy subjects, Williams, Pascual-Leone,
and Fregni (2010) combined bilateral motor cortex tDCS with contralateral
hand restraint of the dominant hand. When comparing active
stimulation to sham stimulation, they found a decrease in cortical excitability
in the dominant hemisphere and a decrease in transcallosal
inhibition from the dominant hemisphere to the non-dominant hemisphere.
The decrease in transcallosal inhibition correlated with motor
performance enhancement in the non-dominant hand (Williams et al.,
2010).

notes:
The different neurochemical
changes observed anodal stimulation
and cathodal stimulation suggest that the excitatory
effects of anodal tDCS are mediated at least in part by a
reduction in GABAergic inhibition in addition to the NMDAreceptor
dependency previously demonstrated , while the inhibitory effects of
cathodal tDCS are mediated by reduction in excitatory glutamatergic
neurotransmission.

*this is picture of old version newer is on manual ,electrodes size and poisition is count only for electrode current density not for current density in the brain and fieled orintation.I working on new better model.

Aplications :

For long term use must be considered side effect form reference electrode and current path in the brain (and many more) ,poreblem is clinical studies didnt look for this effects.

EKG electrode problem i do some test with EKG electrode 3,14cm2 ,1mA , 318uA/cm2 ,+ on L-DLPFC and - on FT10 (left temporal below the hairline)
I try severel things one of them is usage of high current density in electrode 318uA/cm2 , this is show no problem if i rmap is slowly i feel needles on a skin for about 20s and after this nothing(skin been prepared before put electrode).

I left electrode stick to head for 24h and try another stimulation i be curious about waht do skin below electrodes and how sweting and other thiong change function.A ramp it up and strat feel needles so i lowering it down try little adjust electrode contact in tect try is be better but still the feeling start before
reach full current.I use setup for about 6min in lower current (without feeling).Resul of this test shows something is wrong and alectrode have bad contact.

Examinatin of electrodes cathode lost color normaly is back noe have metal color gel have brown color and little bump maybe bubble.Anode looks normal.
This is a problem i plan use Ag/AgCl disk or whole ekg elctrode as HD-TDCS this electrochmicl decompositions means i need use other type.The lectrode is been used for about 25min with large current density with lower can be this effect slower.Theoreticly electrode may work afther this prety weel and problem be probably caused by little bump (different gel my help) and sweting . Some Ag iont maybe go to skin but this is no poroblem maximaly i turn blue (like some guy used to much coloidal silver) the steal below Ag coating may act as electrode weel but the bubble/bump is a large problem its posible it lowering contact area to the skin nad chnged current didtribution in the gell. After test is skin uder lectrodes little red this disapears aftef about 15mins redness is be higher uder catode.

10/10 placemet or better targeting

Definition of problem

How to find specific location ?
How to make a 10/10 precize electrode cap?

TESTING :

Subjective testing

Normal - only turn it on and wait for effect

For me the most important first to determine whether it has any noticeable effect on my consciousness, even if it be only a placebo. If I get effect will be the next phase - more scientific testing.

not scientific method,its a purely subjective measurement

TEST 1

(In fact about 40s but previous tests were from an earlier apparatus and/or were not documented)

20 min stimulation of DLPFC (t 0-20)

25.10 2011 17:06 - 00:36

At the beginning (t -270-0) i was tired poor concentration and stiff neck .My situation is continuously improved in the course of stimulation
i was more aware of surroundings and body ,my concentration improved,fatigue disappeared bud my neck is still little stiff.About 2 mins after stimulation i was almost back in same state that there in the begining.Notice the red line is the stress in the body (mostly stress hormones and negative emotion part of limbic sistem)they block the increase of alertness and it may also start feedback loop leading to fatigue and depression. Small amount of it is enough to block an increase in awerness above normal levels only a strong stimulation overcomes thers effect.
Only way out is stop their production and start cleaning , tDCS do this job for us.After all the stress from the body disappeared awerness began to rise again and a lot more than before .In t 160 very fast change of perception and i began to smile.Production of stress is at 0 maybe this made ​​the change -more research needed . t 180 I smile a lot ,i more aware colors are colorful shapes sharper and the world and somehow more interesting . No I'm not on drugs only tDCS :).Data ends at t+180 i must go to sleep.

TIME
5- and 7-minute tDCS results in after-effects lasting for no longer than
5 minutes, 9- to 13- minute tDCS results in after-effects lasting from 30 to
90 minutes, respectively (Nitsche & Paulus, 2001). Therefore, when we
discuss electrophysiological effects of tDCS it is important to distinguish
between: (1) immediate effects (e.g., anodal tDCS as excitatory, cathodal
tDCS as inhibitory); and (2) the after-effects of stimulation (e.g., facilitation
vs. inhibition of activity) as they may be related to different mechanisms
of action (e.g., membrane vs. synaptic mechanisms).

probably 1mA/35cm2

REPEATING
While the above neurophysiological studies only examined variation
in duration of a single session of tDCS, behavioral evidence suggests that
repeating sessions of tDCS over several consecutive days can enhance the
effects of tDCS as well (Boggio, Nunes et al., 2007). Boggio et al. (2007)
examined improvement of motor performance in stroke patients following
four weekly sessions of tDCS and five consecutive daily sessions of
tDCS. In both experimental paradigms, they found significant motor
function improvement after either cathodal tDCS of the unaffected hemisphere
or anodal tDCS of the affected hemisphere when compared to
sham tDCS. Importantly, while they did not find a significant cumulative
effect associated with weekly sessions of tDCS, consecutive daily sessions
of tDCS were associated with significant improvement over time that was
sustained for 2 weeks after treatment. Future neurophysiological studies
should confirm whether the neuromodulatory effects of tDCS could
indeed be enhanced by consecutive daily sessions.

Nitsche et al. (2007) explored whether tDCS-induced background
network activity changes effect PAS-induced plasticity. They hypothesized
according to homeostatic plasticity theory that the effect of PAS would be
enhanced with decreased background activity (Nitsche et al., 2007).
Administering the PAS protocol to 12 healthy subjects, Nitsche et al.
(2007) slowly stimulated the right ulnar nerve at the wrist at an intensity
300% above sensory threshold while a single TMS pulse was delivered
over the contralateral motor cortical region representing the right abductor
digiti minimi muscle. This protocol was performed alone, following
anodal and cathodal tDCS, and simultaneously with anodal and cathodal
tDCS. When administered simultaneously with PAS, excitability-enhancing
(anodal) tDCS decreased the efficacy of PAS and excitabilitydiminishing
(cathodal) tDCS increased the efficacy of PAS.This same
effect was observed for prolonged administration of tDCS as well, but was
not observed when tDCS was administered before PAS. This suggests, in
accordance with theories of homeostatic plasticity, that tDCS has the
potential to modify the efficacy of PAS by modulating background activity
in the brain. For instance, decreased excitability of the cortex induced
by cathodal tDCS, when applied in combination with PAS, has the
potential to increase associative synaptic plasticity.
*more in study ,find articles

tDCS on conditions such as chronic pain may shed light onto
the neurophysiological mechanisms underlying these effects (see Zaghi
et al., 2010, for recent review of the clinical applications of tDCS).

The v4 is designed to drive higher impedance electrodes in addition to the usual sponge+saline electrodes by using the LT1026 charge pump controller to produce +18V to -18V split source from a 9V battery. It uses the LM334Z IC for fine current limiting control and a JFET as a gross 5mA limiter in case of LM334Z failure. ESD protection comes from two varistors. from:http://wiki.hacdc.org/index.php/TDCS

12.3 2013

Ramping capacitor - possible problem

Yesterday i was bulding some tDCS with LM334 and try for first time use ramping capacitor. When i test device with load (5KOhms) all was ok ramping when i turn device on and ramping down when of. But when i change load (5kOhms potentiometer) during stimulation (testing) it create current peak up to 5 mA. I test it with few different capacitor and behavior is alwayes the same (only diffrent value of peak nad the time to return to normal ). Device without capacitor work witkout poroblem. In resuls of this i use instead of capacitor serail load (bid linear potentiometr 100kOhms ) allows me to do manual ramping (0,07mA to setup current).

My question is can anybody test this capacitor problem maybe i do semething wrong , bad multimetter etc.. . If is this problem real is very bad idea use capacitor for ramping in use the resistance change is not to quick but stil can cause pretty high current peaks.